Introduction: The endothelium plays an important role in maintaining vascular structure and tonus; and endothelial cells are protective against the thrombosis and atherosclerosis. Cardiovascular risk factors, such as metabolic diseases, systemic and local inflammations, result in endothelial dysfunction. Nitric oxide is one of the endothelium derived substances that has an important role in maintaining the endothelial homeostasis. The asymmetric dimethylarginine (ADMA) is the endogenous inhibitor of the nitric oxide synthase. ADMA has been shown to impair the endothelial function and to be associated with hypercholesterolemia, hyperhomocysteinemia, and atherosclerosis. Ascorbic acid, a vitamin with reductant and antioxidant effects, can improve endothelial function and decrease the reactive oxygen species level. Our objective was to determine pathologically exogenous ADMA effect on endothelium of abdominal aorta, and to observe protective effect of antioxidant ascorbic acid. Materials and methods: The rats were divided in three groups: control, ADMA and ADMA + ascorbic acid. After administration of ADMA and ascorbic acid for 10 days, the blood was collected and abdominal aorta removed from the animals. Homocysteine, triglyceride, and cholesterol levels were measured by autoanalyzer. Abdominal aorta was evaluated histopathologically and the intimal thickness was measured using an imaging system. Result: The ADMA increased the intimal thickness (p=0.003), and ascorbic acid inhibited this increase (p=0.001). ADMA also increased the levels of triglyceride and cholesterol (p=0.008 and p=0.001), and the increased triglyceride and cholesterol levels are inhibited by ascorbic acid (p=0.000 and p=0.001). Conclusions: Increased intimal thickness by delivering exogenous ADMA supports that exogenous ADMA might be one of the factors resulting in atherosclerosis. We consider that the increase in intima thickness may not be a direct effect of ADMA but may be secondary to the increased cholesterol levels and ascorbic acid can be protective for atherosclerosis.
Source

Methyl and ethyl alcohol poisoning are still responsible for high morbidity and mortality rates. The purpose of this retrospective study was to examine ethyl and methyl alcohol poisoning related deaths in Ankara and surrounding cities between 2001 and 2011 and compare them with previous studied conducted in Turkey and other countries. For this purpose, 10,720 medico-legal autopsy cases performed in Ankara Branch of the Council of Forensic Medicine were reviewed in terms of alcohol poisonings. The deaths due to methanol and ethanol poisoning were 74 (0.69% of all medico-legal autopsies performed) and the distribution among them was 35 (47.3%) for methanol poisoning and 39 (52.7%) for ethanol poisoning. Overwhelming majority of the cases were male (n = 67, 90.5%). The mean age of the victims was 44.9 ± 10.9 years and ranging from 21 to 92 years. The age group of 35-49 years was the mostly affected. Most of the cases were seen in 2004 (n = 12, 16.2%). The levels of postmortem blood alcohol levels were available for all cases and the mean alcohol levels were 322.8 ± 155.5 mg/dL ranging from 74 to 602 mg/dL for methanol and 396.8 ± 87.1 mg/dL and ranging from 136 to 608 mg/dL for ethanol. Early diagnosis is essential for successful treatment in methanol and ethanol poisoning. Besides increased awareness, more sensitive/specific diagnostic tools, and the prompt approach to the poisoned individual should be implemented in the hospitals.
Source

The endoplasmic reticulum (ER) is related to the various signal routes that are activated in unfolded protein response (UPR). The Grp78, Grp94, CHOP, MTJ1 and HMOX1 genes expressions demonstrate UPR activity. In this study, we investigated the UPR gene expressions in larynx epidermoid carcinoma (HEp2) to which dexamethasone (dex) was applied. HEp2 cells were administered for 48 h with different combinations using 0.1 μM and 1 μM dex, 1 mM phenyl butyric acid (PBA) and 100 ng/ml lipopolysaccharide (LPS). The Grp78, Grp94, CHOP, MTJ1 and HMOX1 genes expression was determined using quantitative RT-PCR. The Grp78, MTJ1 and HMOX1 gene expression increased with the administration of 1 μM dex. CHOP expression, on the other hand, decreased with 0.1 μM dex. When dex was combined with LPS, nearly all gene expressions decreased. The increase in Grp78, Grp94, HMOX1 and MTJ1 gene expression was greater in groups in which dex was administered in combination with PBA than in groups in which dex was administered alone. Dex in low dose (0.1 μM) caused a decrease in CHOP expression in HEp2 cells and an increase in Grp78 expression, in particular. The changes in UPR genes expressions may lead to the extended survival of the cells.
Source